At birth a newborn infant is exposed to the microbiota of the mother, and microbes from the environment, which starts the colonization of mucosal surfaces in the digestive, respiratory and urogenital tracts, and the skin (Calder 2013). This process starts the maturation of the immune system. The colonizing microbiota and the intestinal immune system interact to establish life-time tolerance and mutualism between each other (Tourneur & Chassin 2013). This reciprocal interaction is a life-lasting process that influences the function and homeostasis of our immune system and well-being. Thus the composition and metabolism of the microbiota has direct influence on our immune health from birth to death (Maynard et al 2012). Therefore, modulation of the indigenous intestinal microbiota via the introduction of probiotic strains may play an important role in preventative health and in the management of specific conditions. (Wall et al 2009) The most generally accepted definition of probiotics was proposed by a FAO/WHO work group: “Live microorganisms which when administered in adequate amounts confer a health benefit on the host” (FAO/WHO. Guidelines for the evaluation of probiotics in food 2001. Food and Agriculture Organization of the United Nations (FAO). 2001.). The most commonly used probiotics are lactic acid bacteria, such as those belonging to the genera Lactobacillus and Bifidobacterium. 
Pathogenic viruses have many forms and can cause many effects and symptoms. Furthermore, despite the commonness of viral infections, for most there is little treatment.
Human rhinovirus (HRV) infections are the cause of a common cold, and this disease places a large health and economic burden on society (Heikkinen T, Järvinen A. 2003).
Children have on average 6-8 colds annually and adults 1-4, of which approximately half are caused by the rhinoviruses (Heikkinen T, Järvinen A. 2003).
Usually, common cold itself is a self-limiting illness and will pass by without any medication. However, the symptoms are unpleasant and may last from several days to several weeks.
Rhinoviruses (and many other viruses) are typically caught from the environment by self-inoculation e.g. by touching one's nostril. HRVs then pass the nasal mucus and infect epithelial cells of the airways. The response of the epithelium and innate immune cells causes inflammatory response and secretion of inflammatory mediators such as cytokines and chemokines e.g. IL-1beta, IL-6, RANTES (CCL5), GM-CSF, IP-10, and of note IL-8. These cytokines mediate the attack of the immune cells against the virus infected cells that causes cold symptoms. In healthy subjects HRVs cause an inflammatory response and common cold symptoms that will pass by without any treatment. Similar immune responses occur in response to other virus infections.
HRV infections are associated with exacerbations of asthma, COPD, and idiopathic pulmonary fibrosis (IPF) in subjects suffering from these conditions (Saraya et al. 2014). In approximately 26-36% of asthma, 3-27% of COPD, and 5% of IPF cases HRV infections have been found to cause the exacerbations (Saraya et al. 2014; Table 1). Also other viruses like respiratory syncytial virus (RSV) and influenza are associated with the aetiology (Gunawardana et al. 2014 Antiviral Research). Furthermore, HRV infections together with RSV and metapneumovirus are associated with the early onset of wheezing episodes (bronchiolitis) in children (Saglani 2014). Approximately one-third of children who wheeze in the first 3 years of life continue to wheeze in later life and thus wheezing induced by viral infections or common cold is a risk factor for developing asthma (Sigurs et al. 2010; Jackson et al. 2012).
In asthmatics inflammatory cytokines, including IL-8, are known to worsen the pathology, and neutrophilic, lymphocytic and eosinophilic inflammation with airway hyperresponsiveness and airway remodeling characteristic to asthmatics are observed (Wark et al. 2002; Proud 2011). In asthmatics a deficient anti-viral mechanisms have been found (Contoli 2006) and it has been demonstrated that intranasally inoculated HRV induced clinical illness in asthmatics correlated to viral load and airway inflammation (Message et al. 2008).
There are several placebo-controlled clinical studies that have examined the efficacy of probiotics (Hao 2011; Kang 2014) in relation to common respiratory tract illness symptoms. These studies indicate that probiotic supplementation may reduce the incidence, and duration of illness in comparison to placebo supplements (Hao 2011 Kang 2014). However, these studies have only studied the symptoms of respiratory illness, not the causative agents, like viruses.
Clinical trials have looked at the efficacy of probiotics against the development of childhood asthma, but none of the studies have looked at the association of rhinoviruses with the asthma development (Azad 2013; Elazab 2013).
In COPD subjects, studies have found a role for inflammatory mediators in exacerbations and a clear association with viral infections exists (Gunawardana et al. 2014). A research team tested patients with mild COPD in an experimental rhinovirus model where HRV was inoculated to many of the noses of the volunteers; viral titers and inflammation were followed (Mallia et al. 2013). They demonstrated that IL-8 levels were higher in COPD patients than in healthy controls. Furthermore in nasal lavage of the COPD patients virus titer was found higher than in healthy controls (Gunawardana et al. 2014) that indicate deficient anti-viral defense mechanisms in COPD patients. Thus inflammation (indicated by IL-8) and viral titers are higher in COPD patients.
The inventors have surprisingly found that use of bifidobacteria modulates the immune system to not only affect viral action, but also reduce viral effects such as inflammation. Furthermore, in having this action the compositions of the current invention help in alleviating asthma and COPD exacerbations, and also reduce the risk of virus infection, such as HRV infection, that predisposes the subject to development of asthma or COPD in susceptible individuals.